MMG test 2

Opsonization

the process of coating a pathogen so immune cells can recgonize and engulf it more easily

opsonin

a substance that coats a pathogen and promotes phagocytosis, such as antibodies or complement protein C3b

antigen

a substance specifically recognized by an antibody or immune receptors

some trigger an immune response while others don’t

cytokine

a signaling protein released by cells that regulates immune responses and communication between cells

epitope

the specific part of an antigen that an antibody or immune receptor recognizes

also called antigenic determinant

interferon

a cytokine that helps protect cells against viral infection and coordinates immune defenses

margination

the movement of leukocytes toward the inner surface of blood vessels during inflammation

diapedesis

the movement of leukocytes blood vessels walls into infected or injured tissues

also called extravasation

pyrogen

a substance that causes fever by promoting an increase in the body’s temperature set point

plasma

liquid portion of blood that contains clotting factors

obtained from blood collected with an anticoagulant

contains fibrinogen and other clotting proteins

contains water, electrolytes, proteins, hormones, and antibodies

serum

liquid remaining after blood as clotted

obtained from clotted blood

has little to no fibrinogen because it was used during clotting

contains many of the same substances including antibodies

what are the three immune cells that are phagocytes

neutrophils, macrophages, and dentritic cells

neutrophils

phagocyte, usually the first leukocytes recruited to an acute infection

rapidly engulf and destroy microbes

macrophage

phagocyte, develop from monocytes or from tissue-resident populations

engulf pathogens, remove dead cells, release cytokines, help coordinate inflammation

dendritic cells

phagocyte, capture antigens in tissues and present them to T cells

helps connect innate and adaptive immunity

steps to phagocytosis

step 1: recognition and attachment

step 2: engulfment

step 3: digestion

step 4: disposal and signaling

what is phagocytosis’s role in innate immunity

phagocytosis rapidly removes invading microbes

limits spread, clears damaged cells, and helps initiate inflammation

two ways phagocytosis recgonizes pathogens

1. pattern recognition receptors (PRRs)- recognize common microbial structures called pathogen-associated molecular patterns (PAMPs)

2. opsonin receptors- recognize substance coating pattern, making engulfment easier

types of cytokines

interferons, interleukins, tumor necrosis factor, chemokines, colony-stimulating factors

interferon

establish antiviral defenses in cells

supports cell-mediated immunity

interleukins

coordinate communication, growth, activation, an differentiation of immune cells

tumor necrosis factor

promotes inflammation, activates vascular endothelium and can contribute to fever

chemokines

attact immune cells toward infection or injury through chemical gradients

colony-stimulating factors

promote the production and development of blood cells in the bone marrow

paracine

on nearby cells

endocrine

at distant sites through circulation

complement system

a group of proteins in blood and tissues that activate in a cascade to help eliminate pathogens

part of innate immune system

functions: opsonization, inflammation, lysis

body temp protects humans against which type of microbe

temperature sensitive microbes

reasons why an immune response to an infection makes you tired

cytokine release- promotes sickness behavior, sleepy and fatigue

energy redistribution- the body may reduce energy spent on other activities to save it for the immune cells

Sleep and metabolic changes- inflammation alters sleep regulation

innate immunity

minutes to hours

recognizes broad patterns

no memory

adaptive immunity

days

recognizes particular antigens and epitopes

long lasting memory

B cells, T cells, antibodies

first line of defense

skin, mucous membranes

second line of defense

phagocytes, inflammation, fever, innate defenses

third line of defense

antigen-specific adaptive immunity

how do normal microbiota protect against pathogens

colonization resistence- compete with pathogens for nutrients and attachment sites, change local conditions

lysozyme

an enzyme that breaks bonds in peptidoglycan

helps weakens bacterial cell walls

found in tears, saliva, mucus, breast milk

works well against gram-positive bacteria

antimicrobial peptides

small molecules that directly damage microbes or interfere with their growth

lymph

interstitial fluid that enters lymphatic vessels

contains water, dissolved substances, immune cells, and fats

filtered by lymph nodes

primary lymphoid tissues

develop lymphocytes

bone marrow- produce blood cells, where b cells mature

thymus- where t cell mature

secondary lymphoid tissues

where mature lymphocytes encounter antigens and become activated

lymph nodes- filter lymph, provide sites for lymphocyte activation

spleen- filters blood, responds to blood-borne antigens

MALT- defends mucosal surfaces

leukocytes

white blood cells

what are the two categories of leukocytes

agranulocytes- lack prominent specific granules, lymphocytes, monocytes

granulocytes- have prominent cytoplasmic granules, neutrophils, eosinophils, basophils

granulocytes

Leukocyte

have prominent cytoplasmic granules

neutrophils, eosinophils, basophils

agranulocytes

Leukocyte

lack prominent specific granules

lymphocytes, monocytes

monocytes

agranulocyte

circulate in blood

can differentiate into macrophages or dendritic cells

macrophages

engulf pathogens and debris

produce cytokines

tissue repair

dendritic cells

capture antigens

transport antigen information from peripheral tissues to lymphoid organs

what are the 3 types of lymphocytes

B cells

T cells

T killer cells

B cells

mature in bone marrow

differentiate into plasma cells

can form memory B cells

T cells

mature in thymus

T helper cells and cytotoxic T cells

coordinate immunity or directly kill and abnormal cells

why leukocytes are central to second-line molecular defenses

they detect threat, release cytokines, engulf microbes, kill infected cells, and coordinate other defenses

3 primary function and phases of inflammation

Functions:

1. eliminate or contain the source of injury or infection

2. recruit immune cells and molecules to the affected tissue

3. begin cleaning, healing, and tissue repair

Phases:

1. vasodilation and increase vascular permeability

2. leukocyte recruitment

3. elimination and repair

cardinal signs of inflammation

redness, heat, swelling, pain

chronic inflammation

prolonged inflammation that can last weeks, months, or longer

fever

regulated rise in body temperature caused from an infection or inflammation

fever treatment

fluids, rest, comfortable clothing

continuous fever

temperature remains elevated with relatively little fluctuation

remittent fever

temperature fluctuates considerably but does not return to normal

intermittent fever

temperature rises and falls to normal at least once during the observation period

relapsing fever

episodes of fever are separated by periods of normal temperature lastign longer than a typical daily fluctuation

recurrent fever

fever returns in distinct episodes after period without fever

biphasic

two distinct fever peaks or phases occur during an illness

antigen

a substance recognized by a specific antibody or immune receptor

epitope

the specific portion of an antigen recognized by an immune receptor or antibody

immunogen

a substance capable of triggering an adaptive immune response

all immunogens are antigens but not all antigens are immunogens

HLA

human leukocyte antigen

the human version of NHC system

HLA molecules help present antigens to T cells

MHC

Major Histocompatibility Complex

molecules that display peptide fragments for recognition by T cells

Specificity

immune receptors recognize particular antigens or epitopes

targets the correct antigen

Memory

Memory B and T cells can produce faster and stronger response upon re-exposure to the same antigen

improves future responses

tolerance

the immune system avoids attacking the body’s own tissues under normal conditions

prevents inappropriate attacks on self

MHC 1

expression: nearly all nucleated cells

purpose: identify infected or abnormal cells

CD8- cytotoxic T cells

MHC 2

expression: professional antigen-presenting cells (APCs)

purpose: coordinate immune responses to captured antigens

CD4- helper T cells

processing and presenting intercellular antigens

Endogenous (intracellular) → MHC I → CD8

1. proteins inside cell are broken into peptides

2. peptides enter the endoplasmic reticulum through TAP

3. peptides bind MHC 1 molecules

4. The MHC1- peptide complex moves to cell surface

5. CD8+ T cells inspect the displayed peptide

6. activated cytotoxic T cells can kill cells displaying. the recgonized pathogen

processing and presenting extracellular antigen

Exogenous (extracellular) → MHC II → CD4

1. APC takes up an extracellular pathogen or protein through phagocytosis/endocytosis

2. antigen is broken down inside an intracellular vesicle

3. MHC 2 molecules are produced and transported through the cell’s internal membrane system

4. the invariant chain directs MHC 2 trafficking and protects its peptide-binding groove

5. antigen-derived peptide complex reaches the cell surface

6. CD4+ helper T cells recgonize the complex and may become activated

antigen presenting cells (APCs) role

capture, process, and display foreign antigens in their surface MHC molecules to activate adaptive immune responses

types of APCs (antigen presenting cells)

dendritic cells- activate T cells and initiate adaptive immunity

macrophages- engulf pathogens and debris

B cells- bind to specific antigen and present peptide fragments on MHC 2 helper T cells

TCR (T cell receptors)

number of peptide chains- 2

epitope binding site- 1

interaction with MHC- requires MHC to recognize conventional antigen

BCR (B cell receptors)

number of peptide chains- 2

epitope binding site- 2

interaction with MHC- doesn’t require MHC to recognize conventional antigen

ways antibodies help eliminate specific pathogens

1. neutralization

2. opsonization

3. complement activation

how are T helper cells different from cytotoxic T cells

T helper cells: CD4, peptide on MHC 2, coordinate immune responses

Cytotoxic T cells: CD8, peptide on MHC 1, kill infected cells

how T helper cells and B cells are activated and how that leads
to destruction of extracellular pathogens

1. B cell recognizes an intact antigen

2. B cell processes the antigen

3. Helper T cells recognizes the peptide

4. Helper T cell provides help

5. B cell proliferates and differentiates

6. antibodies help eliminate pathogens

cell mediated immunity

Main cells: T cells

Main effectors: cytotoxic T cells and activated macrophages

Best suited for: intracellular infections, infected cells

Antigen recognition: TCRs recognize peptide-MHC complexes

Memory: memory T cells

Humoral Immunity

Main cells: B cell and plasma cells

Main effectors: antibodies

Best suited for: extracellular microbes and toxins

Antigen recognition: BCRs bind to intact antigens

Memory: Memory B cells and long-lived antibody producing plasma cells

IgA

mucosal protection

• saliva, tears, mucus, breast milk

• dimer in secretion

IgM

first major antibody response

• great at agglutination and activating the classical complement pathway

• pentamer secretion

IgG

major blood antibody

• monomer and most abundant antibody class in serum

• important for neutralizing, opsonization, and complement activation

• can cross placenta, passive immunity

• prominent in secondary immune responses

IgE

allergy and parasite defense

• monomer

• binds to mast cells

• helps defend against certain parasitic worms

isotype switching

allows an activated B cell to change the class of antibody it produces

ex. switch from IgM to IgG

why does isotype switching matter in serology testing

serology tests blood for antibodies against particular antigens

a positive test can indicate previous exposure, vaccinations, curretn infection, past infection

4 categories of adaptive immunity

naturally acquired active: long term protection (recovering from chicken pox)

artificially acquired active: long term protection (vaccine)

naturally acquired passive: no lasting memory (passive immunity, received from mother)

artificially acquired passive: temporary memory, no lasting memory (rabies immunoglobulin)

vaccine hesitancy

delay in accepting or a reluctance to accept vaccination despite the availability of vaccination services

mode of transmission for small pox

inhalation of infectious respiratory droplets

direct contact with leasions

incubation period of small pox

10-14 days

tropism of small pox

narrow

highly host specific

exclusively infects humans in nature

2 innate immune defenses that small pox inactivates

interferons

compliment-mediated defenses

initial APC infected by small pox

dendritic cells

mortality rate of small pox

30%

reservoir of small pox

humans

year of eradication of small pox

1980

why vaccine-preventable disease can re-emerge

declining vaccination rates

reduced herd immunity

international travel

vaccine hesitency